Capsaicin prevents the hyperalgesia induced by peripheral group I mGluRs activation.

Group 1 metabotropic glutamate receptors (mGluRs) are expressed in peripheral and central neural tissues and involved in peripheral and central sensitization in various pain models. However, there are limited reports that activation of peripheral group I mGluRs could evoke pain. Furthermore, any behavioral evidences could not be found out, showing what kind of afferent fibers are involved in peripheral mGluRs-mediated hyperalgesia. This study was undertaken to clarify whether peripherally injected group I mGluRs agonists could induce pain-related behaviors and capsaicin-sensitive afferent fibers might be involved in the hyperalgesia. To assess pain sensitivity, mechanical threshold for paw withdrawal response (PWT) was measured and number of spontaneous flinching behavior was counted. Intraplantar injection of group I mGluR agonist, (RS)-3,5-dihydroxyphenylglycine (DHPG) and mGluR5 agonist, (RS)-2-chloro-5-hydroxyphenyglycine (CHPG) immediately induced pain-like behaviors, such as decrease of PWT and increased number of flinchings. These agonists-induced pain-like behaviors were blocked by group I mGluRs antagonist, (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA) and mGluR5 antagonist, 2-methyl-6-(phenylethynyl) pyridine hydrochloride (MPEP). Perineural pretreatment of 1% capsaicin solution significantly reduced pain-related behaviors induced by DHPG and CHPG, proposing that capsaicin-sensitive primary afferent fibers could be responsible for the hyperalgesia induced by activation of peripheral group I mGluRs. This study presents the first behavioral evidence that peripheral group I mGluRs activation could induce spontaneous as well as mechanical hyperalgesia and capsaicin-sensitive afferent fiber could be implicated the group I mGluR mediated hyperalgesia.

The clinical significance of serum and urinary neopterin levels in several renal diseases.

Neopterin is a pyrazino-pyrimidine compound, and is known to be a marker associated with cell-mediated immunity in various diseases. We hypothesized that the levels of serum and urine neopterin would be elevated in renal disease, and would correlate with certain clinical parameters. We evaluated serum and urinary neopterin levels in patients with several renal diseases, including nephrotic syndrome (NS, n=19), chronic renal failure (CRF, n=8), end stage renal disease (ESRD, n=64) and controls (n=22). Serum neopterin was elevated in patients with CRF and ESRD, as compared to controls. Urinary neopterin levels were also found to be elevated in patients with CRF and ESRD, as compared to controls. Serum neopterin levels showed significant positive correlation with age, serum BUN and creatinine levels, and inverse correlation with WBC, hemoglobin, hematocrit, serum albumin and total iron binding capacity. Urine neopterin levels exhibited positive correlation with age and serum creatinine levels, and inverse correlation with WBC, hemoglobin, hematocrit, BUN and serum albumin. In conclusion, increased serum and urinary neopterin levels were found in some patients with renal disease and were correlated with certain clinical parameters.

Eosinophilic peritonitis in a patient with continuous ambulatory peritoneal dialysis (CAPD).

Eosinophilic peritonitis is defined as when there are more than 100 eosinophils present per milliliter of peritoneal effluent, of which eosinophils constitute more than 10% of its total WBC count. Most cases occur within the first 4 weeks of peritoneal catheter insertion and they usually have a benign and self-limited course. We report a patient of eosinophilic peritonitis that was successfully resolved without special treatment. An 84-year-old man with end stage renal disease secondary to diabetic nephropathy was admitted for dyspnea and poor oral intake. Allergic history was negative. and physical examination was unremarkable. Complete blood count showed a hemoglobin level of 11.1 g/dL, WBC count was 24,500/mm3 (neutrophil, 93%; lymphocyte, 5%; monocyte, 2%), platelet count was 216,000/mm3, serum BUN was 143 mg/dL, Cr was 5.7 mg/dL and albumin was 3.5 g/dL. Creatinine clearance was 5.4 mL/min. Three weeks after peritoneal catheter insertion, he was started on peritoneal dialysis with a 6-hour exchange of 2L 1.5% peritoneal dialysate. After nine days, he developed turbid peritoneal effluents with fever (38.4 degrees C), abdominal pain and tenderness. Dialysate WBC count was 180/mm3 (neutrophil, 20%; lymphocyte, 4%; eosinophil, 76% [eosinophil count: 136/mm3]). Cultures of peritoneal fluid showed no growth of aerobic or anaerobic bacteria, or of fungus. Continuous ambulatory peritoneal dialysis (CAPD) was commenced, and he was started on intraperitoneal ceftazidime (1.0 g/day) and cefazolin (1.0 g/day). After two weeksr, the dialysate had cleared up and clinical symptoms were improved. Dialysate WBC count decreased to 8/mm3 and eosinophils were not detected in peritoneal fluid. There was no recurrence of eosinophilic peritonitis on follow-up evaluation, but he died of sepsis and pneumonia fifteen weeks after admission.